Abstract

Amiodarone, an iodinated antiarrhythmic agent, has complex effects on thyroid hormone physiology. As a potent hepatic 5′-deiodinase inhibitor, the drug decreases thyroxine (T4) conversion to 3,5,3′-triiodothyronine (T3), and slows 3,3′,5′-triiodothyronine (rT3) clearance (1-3). Amiodarone may inhibit both the cellular uptake of T3 and T4 (4, 5), and the binding of T3 to its receptor (5, 6). These effects modulate T3-mediated responses in vitro (5-7) and in animals (8). Finally, iodide released from metabolism of the drug may occasionally cause overt hypothyroidism or hyperthyroidism (9). Given the antagonistic effects of amiodarone on T3 action, we studied whether the drug could elevate